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LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer
Chemoresistance is a huge clinical challenge in the treatment of advanced colorectal cancer (CRC). Non-coding RNAs (ncRNAs) and messenger RNA (mRNA) are involved in CRC chemoresistance. However, the profiles of long ncRNAs (lncRNAs), microRNAs (miRNAs), mRNAs and competing endogenous RNA (ceRNA) net...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9587682/ https://www.ncbi.nlm.nih.gov/pubmed/35914269 http://dx.doi.org/10.1093/carcin/bgac065 |
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author | Yao, Fei Huang, Xiaoying Xie, Zhufu Chen, Jie Zhang, Ling Wang, Qiang Long, Hui Jiang, Jue Wu, Qingming |
author_facet | Yao, Fei Huang, Xiaoying Xie, Zhufu Chen, Jie Zhang, Ling Wang, Qiang Long, Hui Jiang, Jue Wu, Qingming |
author_sort | Yao, Fei |
collection | PubMed |
description | Chemoresistance is a huge clinical challenge in the treatment of advanced colorectal cancer (CRC). Non-coding RNAs (ncRNAs) and messenger RNA (mRNA) are involved in CRC chemoresistance. However, the profiles of long ncRNAs (lncRNAs), microRNAs (miRNAs), mRNAs and competing endogenous RNA (ceRNA) networks in CRC chemoresistance are still largely unknown. Here, we compared the gene expression profiles in chemosensitive (HCT8) and chemoresistant [HCT8/5-fluorouracil (5-Fu) and HCT8/cisplatin (DDP)] cell lines by whole-transcriptome sequencing. The common differentially expressed RNAs in two drug-resistant cells were selected to construct lncRNA–miRNA–mRNA networks. The ceRNA network closely related to chemoresistance was further established based on the widely accepted drug resistance-associated genes enriched in three signaling pathways involved in chemoresistance. In total 52 lncRNA–miRNA–mRNA pathways were screened out, among which EPHA2 and LINC02418 were identified as hub genes; thus, LINC02418/miR-372-3p/EPHA2 were further selected and proved to affect the 5-Fu and DDP resistance of CRC. Mechanistically, LINC02418 upregulated EPHA2 by functioning as a ‘sponge’ of miR-372-3p to modulate the chemoresistance of CRC. Collectively, our study uncovered the underlying mechanism of LINC02418/miR-372-3p/EPHA2 in 5-Fu and DDP resistance of CRC, which may provide potential therapeutic targets for improving the chemosensitivity of CRC. |
format | Online Article Text |
id | pubmed-9587682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-95876822022-10-25 LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer Yao, Fei Huang, Xiaoying Xie, Zhufu Chen, Jie Zhang, Ling Wang, Qiang Long, Hui Jiang, Jue Wu, Qingming Carcinogenesis Carcinogenesis Chemoresistance is a huge clinical challenge in the treatment of advanced colorectal cancer (CRC). Non-coding RNAs (ncRNAs) and messenger RNA (mRNA) are involved in CRC chemoresistance. However, the profiles of long ncRNAs (lncRNAs), microRNAs (miRNAs), mRNAs and competing endogenous RNA (ceRNA) networks in CRC chemoresistance are still largely unknown. Here, we compared the gene expression profiles in chemosensitive (HCT8) and chemoresistant [HCT8/5-fluorouracil (5-Fu) and HCT8/cisplatin (DDP)] cell lines by whole-transcriptome sequencing. The common differentially expressed RNAs in two drug-resistant cells were selected to construct lncRNA–miRNA–mRNA networks. The ceRNA network closely related to chemoresistance was further established based on the widely accepted drug resistance-associated genes enriched in three signaling pathways involved in chemoresistance. In total 52 lncRNA–miRNA–mRNA pathways were screened out, among which EPHA2 and LINC02418 were identified as hub genes; thus, LINC02418/miR-372-3p/EPHA2 were further selected and proved to affect the 5-Fu and DDP resistance of CRC. Mechanistically, LINC02418 upregulated EPHA2 by functioning as a ‘sponge’ of miR-372-3p to modulate the chemoresistance of CRC. Collectively, our study uncovered the underlying mechanism of LINC02418/miR-372-3p/EPHA2 in 5-Fu and DDP resistance of CRC, which may provide potential therapeutic targets for improving the chemosensitivity of CRC. Oxford University Press 2022-08-01 /pmc/articles/PMC9587682/ /pubmed/35914269 http://dx.doi.org/10.1093/carcin/bgac065 Text en © The Author(s) 2022. Published by Oxford University Press. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Carcinogenesis Yao, Fei Huang, Xiaoying Xie, Zhufu Chen, Jie Zhang, Ling Wang, Qiang Long, Hui Jiang, Jue Wu, Qingming LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer |
title | LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer |
title_full | LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer |
title_fullStr | LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer |
title_full_unstemmed | LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer |
title_short | LINC02418 upregulates EPHA2 by competitively sponging miR-372-3p to promote 5-Fu/DDP chemoresistance in colorectal cancer |
title_sort | linc02418 upregulates epha2 by competitively sponging mir-372-3p to promote 5-fu/ddp chemoresistance in colorectal cancer |
topic | Carcinogenesis |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9587682/ https://www.ncbi.nlm.nih.gov/pubmed/35914269 http://dx.doi.org/10.1093/carcin/bgac065 |
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